The composition of the invention can be used for the treatment of metabolic and toxic liver disorders in human and veterinary medicine. It is especially effective for the treatment of alcoholic and toxic liver disorders, hyperammonemia, abstinence syndromes and alcohol delirium, as well as acute and chronic cerebral hypoxia.
Long-alcoholism and/or stress can give rise to a multiplicity of liver disorders. The psychological changes range from simple fatty liver syndromes through a variety of stages of alcohol hepatitis through fibrosis to cirrhosis of the liver.
During alcoholic degradation, the NAD (nicotinamide-adenosine-dinucleotide) proton acceptor is reduced to NADH. Because of the increase in the amount of NADH as a result, the NADH/NAD ratio is increased which limits the citric acid cycle (Krebs cycle).
The deficiency of NAD, limits gluconeogenesis from amino acids.
The alcohol is degraded by the following enzymes: alcohol dehydrogenase, MFOS (mixed-function oxidation system), catalase, NADP (nicotinamide-adenosine-dinucleotide phosphate)-oxidase, xanthinoxidase.
During the breakdown of the alcohol by means of xanthinoxidase and catalase, hydrogen peroxide is produced which liberates free oxygen radical. Acetaldehyde is the end product of all of these metabolic processes. In the degradation of acetaldehyde, the oxygen radical is the main metabolite and causes lipid oxidation.
It has long been believed, in connection with the treatment of alcohol-related states and associated liver disorders, that one must first take into consideration two toxic products, namely, free oxygen radical and acetaldehyde. To combat their toxic effects, the reduced forms of glutathione and other amino acids containing thiol groups, play a very great role. Hepatoxicity and the decrease in glutathione concentrations are directly proportional.